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Retinoic acid (simplified nomenclature for all-trans-retinoic acid) is a metabolite of vitamin A 1 (all-trans-retinol) that is required for embryonic development, male fertility, regulation of bone growth and immune function. [2] All-trans-retinoic acid is required for chordate animal development, which includes all higher animals from fish to ...
Retinol and retinoic acid play crucial roles in the modulation of gene expression and overall development of an embryo. However, deficit or excess of either one of these substances can cause early embryo mortality or developmental malformations.
Retinoic acid, an important signaling molecule needed throughout embryogenesis, acts through the Hox genes. It was originally postulated that retinoic acid acts to induce the Hoxb-8 gene, [11] but this hypothesis has not been supported by genetic studies in mouse embryos lacking retinoic acid synthesis that still express Hoxb-8 in the limb. [8]
Retinoic acid (RA) is significant in embryonic development. It induces the function of limb patterning of a developing embryo in species such as mice and other vertebrate limbs. [ 51 ]
During development, retinoic acid, a metabolite of vitamin A, is used to stimulate the growth of the posterior end of the organism. [12] Retinoic acid binds to retinoic acid receptors that acts as transcription factors to regulate the expression of Hox genes. Exposure of embryos to exogenous retinoids especially in the first trimester results ...
Establishment of the forelimb field (but not hindlimb field) requires retinoic acid signaling in the developing trunk of the embryo from which the limb buds emerge. [ 2 ] [ 3 ] Also, although excess retinoic acid can alter limb patterning by ectopically activating Shh or Meis1/Meis2 expression, genetic studies in mouse that eliminate retinoic ...
This endoplasmic reticulum protein acts on retinoids, including all-trans-retinoic acid (RA), with both 4-hydroxylation and 18-hydroxylation activities. This enzyme regulates the cellular level of retinoic acid which is involved in regulation of gene expression in both embryonic and adult tissues.
Although endogenous retinoic acid is required in higher vertebrates to limit the caudal Fgf8 domain needed for somitogenesis in the trunk (but not tail), some studies also point to a possible role of retinoic acid in ending somitogenesis in vertebrates that lack a tail (human) or have a short tail (chick). [16]